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Fig. 8 | Molecular Cancer

Fig. 8

From: hsa_circ_0007919 induces LIG1 transcription by binding to FOXA1/TET1 to enhance the DNA damage response and promote gemcitabine resistance in pancreatic ductal adenocarcinoma

Fig. 8

Gemcitabine induces hsa_circ_0007919 expression through enhancing QKI-mediated back-splicing

(A) Correlation analysis of QKI and hsa_circ_0007919 expression in GEM-resistant PDAC tissues. (B-C) Expression of hsa_circ_0007919 and ABR in GEM-resistant PDAC cells with or without QKI inhibition. (D-E) Expression of QKI in normal and GEM-resistant PDAC cells. (F-G) RIP assay analysis of the interaction between QKI and introns of ABR pre-mRNA in normal and GEM-resistant PDAC cells. (H) Schematic representation showing that GEM enhances interaction between QKI and ABR pre-mRNA and promotes back-splicing and cyclization of hsa_circ_0007919. Highly expressed hsa_circ_0007919 recruits FOXA1 and TET1 to mediate de-methylation and transcription of LIG1 and upregulates the expression of LIG1. Overexpression of LIG1 activates base excision repair, mismatch repair and nucleotide excision repair pathways to inhibit the DNA damage and apoptosis of GEM-resistant PDAC cells. Data are the means ± SDs (n = 3 independent experiments), ** p < 0.01, *** p < 0.001

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Molecular Cancer

ISSN: 1476-4598